lncRNA SNHG1 regulates odontogenic differentiation of human dental pulp stem cells via miR-328-3p/Wnt/[beta]-catenin pathway

Background Elucidating the mechanism of odontogenic differentiation of human dental pulp stem cells (hDPSCs) is the key to in-depth mastery and development of regenerative endodontic procedures (REPs). In odontogenic differentiation, lncRNAs have a regulatory role. The goal of this research is to de...

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Veröffentlicht in:Stem cell research & therapy 2022-07, Vol.13 (1)
Hauptverfasser: Fu, Tingting, Liu, Yiran, Huang, Xin, Guo, Yan, Shen, Jiaping, Shen, Hong
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Liu, Yiran
Huang, Xin
Guo, Yan
Shen, Jiaping
Shen, Hong
description Background Elucidating the mechanism of odontogenic differentiation of human dental pulp stem cells (hDPSCs) is the key to in-depth mastery and development of regenerative endodontic procedures (REPs). In odontogenic differentiation, lncRNAs have a regulatory role. The goal of this research is to determine the involvement of short nucleolar RNA host gene 1 (SNHG1) in hDPSCs' odontogenic differentiation and the mechanism that underpins it. Methods hDPSCs were isolated from the dental pulp tissue of healthy immature permanent teeth. Follow-up experiments were performed when the third generation of primary cells were transfected. The proliferation ability was measured by CCK-8. The biological effects of SNHG1 and miR-328-3p were determined by real-time quantitative polymerase chain reaction (qRT-PCR), western blot (WB), alkaline phosphatase (ALP) staining and activity, alizarin red S staining (ARS) and quantification, and immunofluorescence staining. The binding of SNHG1 and miR-328-3p was confirmed using a dual-luciferase reporter assay. qRT-PCR and WB were used to determine whether the canonical Wnt/[beta]-catenin pathway was activated. Results On the 0th, 3rd, and 7th days of odontogenic differentiation of hDPSCs, SNHG1 showed a gradual up-regulation trend. SNHG1 overexpression enhanced the mRNA and protein expression of dentin sialophosphoprotein (DSPP), dentine matrix protein 1 (DMP-1) and ALP. We found that SNHG1 could bind to miR-328-3p. miR-328-3p inhibited the odontogenic differentiation of hDPSCs. Therefore, miR-328-3p mimics rescued the effect of SNHG1 overexpression on promoting odontogenic differentiation. In addition, SNHG1 inhibited Wnt/[beta]-catenin pathway via miR-328-3p in odontogenic differentiation of hDPSCs. Conclusion lncRNA SNHG1 inhibits Wnt/[beta]-catenin pathway through miR-328-3p and then promotes the odontogenic differentiation of hDPSCs. Keywords: lncRNA SNHG1, Odontogenic differentiation, hDPSCs, miR-328-3p, Wnt/[beta]-catenin
doi_str_mv 10.1186/s13287-022-02979-w
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In odontogenic differentiation, lncRNAs have a regulatory role. The goal of this research is to determine the involvement of short nucleolar RNA host gene 1 (SNHG1) in hDPSCs' odontogenic differentiation and the mechanism that underpins it. Methods hDPSCs were isolated from the dental pulp tissue of healthy immature permanent teeth. Follow-up experiments were performed when the third generation of primary cells were transfected. The proliferation ability was measured by CCK-8. The biological effects of SNHG1 and miR-328-3p were determined by real-time quantitative polymerase chain reaction (qRT-PCR), western blot (WB), alkaline phosphatase (ALP) staining and activity, alizarin red S staining (ARS) and quantification, and immunofluorescence staining. The binding of SNHG1 and miR-328-3p was confirmed using a dual-luciferase reporter assay. qRT-PCR and WB were used to determine whether the canonical Wnt/[beta]-catenin pathway was activated. Results On the 0th, 3rd, and 7th days of odontogenic differentiation of hDPSCs, SNHG1 showed a gradual up-regulation trend. SNHG1 overexpression enhanced the mRNA and protein expression of dentin sialophosphoprotein (DSPP), dentine matrix protein 1 (DMP-1) and ALP. We found that SNHG1 could bind to miR-328-3p. miR-328-3p inhibited the odontogenic differentiation of hDPSCs. Therefore, miR-328-3p mimics rescued the effect of SNHG1 overexpression on promoting odontogenic differentiation. In addition, SNHG1 inhibited Wnt/[beta]-catenin pathway via miR-328-3p in odontogenic differentiation of hDPSCs. Conclusion lncRNA SNHG1 inhibits Wnt/[beta]-catenin pathway through miR-328-3p and then promotes the odontogenic differentiation of hDPSCs. Keywords: lncRNA SNHG1, Odontogenic differentiation, hDPSCs, miR-328-3p, Wnt/[beta]-catenin</description><identifier>ISSN: 1757-6512</identifier><identifier>EISSN: 1757-6512</identifier><identifier>DOI: 10.1186/s13287-022-02979-w</identifier><language>eng</language><publisher>BioMed Central Ltd</publisher><subject>Genetic research ; Phosphatases ; RNA ; Stem cells</subject><ispartof>Stem cell research &amp; therapy, 2022-07, Vol.13 (1)</ispartof><rights>COPYRIGHT 2022 BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,864,27924,27925</link.rule.ids></links><search><creatorcontrib>Fu, Tingting</creatorcontrib><creatorcontrib>Liu, Yiran</creatorcontrib><creatorcontrib>Huang, Xin</creatorcontrib><creatorcontrib>Guo, Yan</creatorcontrib><creatorcontrib>Shen, Jiaping</creatorcontrib><creatorcontrib>Shen, Hong</creatorcontrib><title>lncRNA SNHG1 regulates odontogenic differentiation of human dental pulp stem cells via miR-328-3p/Wnt/[beta]-catenin pathway</title><title>Stem cell research &amp; therapy</title><description>Background Elucidating the mechanism of odontogenic differentiation of human dental pulp stem cells (hDPSCs) is the key to in-depth mastery and development of regenerative endodontic procedures (REPs). In odontogenic differentiation, lncRNAs have a regulatory role. The goal of this research is to determine the involvement of short nucleolar RNA host gene 1 (SNHG1) in hDPSCs' odontogenic differentiation and the mechanism that underpins it. Methods hDPSCs were isolated from the dental pulp tissue of healthy immature permanent teeth. Follow-up experiments were performed when the third generation of primary cells were transfected. The proliferation ability was measured by CCK-8. The biological effects of SNHG1 and miR-328-3p were determined by real-time quantitative polymerase chain reaction (qRT-PCR), western blot (WB), alkaline phosphatase (ALP) staining and activity, alizarin red S staining (ARS) and quantification, and immunofluorescence staining. The binding of SNHG1 and miR-328-3p was confirmed using a dual-luciferase reporter assay. qRT-PCR and WB were used to determine whether the canonical Wnt/[beta]-catenin pathway was activated. Results On the 0th, 3rd, and 7th days of odontogenic differentiation of hDPSCs, SNHG1 showed a gradual up-regulation trend. SNHG1 overexpression enhanced the mRNA and protein expression of dentin sialophosphoprotein (DSPP), dentine matrix protein 1 (DMP-1) and ALP. We found that SNHG1 could bind to miR-328-3p. miR-328-3p inhibited the odontogenic differentiation of hDPSCs. Therefore, miR-328-3p mimics rescued the effect of SNHG1 overexpression on promoting odontogenic differentiation. In addition, SNHG1 inhibited Wnt/[beta]-catenin pathway via miR-328-3p in odontogenic differentiation of hDPSCs. Conclusion lncRNA SNHG1 inhibits Wnt/[beta]-catenin pathway through miR-328-3p and then promotes the odontogenic differentiation of hDPSCs. 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In odontogenic differentiation, lncRNAs have a regulatory role. The goal of this research is to determine the involvement of short nucleolar RNA host gene 1 (SNHG1) in hDPSCs' odontogenic differentiation and the mechanism that underpins it. Methods hDPSCs were isolated from the dental pulp tissue of healthy immature permanent teeth. Follow-up experiments were performed when the third generation of primary cells were transfected. The proliferation ability was measured by CCK-8. The biological effects of SNHG1 and miR-328-3p were determined by real-time quantitative polymerase chain reaction (qRT-PCR), western blot (WB), alkaline phosphatase (ALP) staining and activity, alizarin red S staining (ARS) and quantification, and immunofluorescence staining. The binding of SNHG1 and miR-328-3p was confirmed using a dual-luciferase reporter assay. qRT-PCR and WB were used to determine whether the canonical Wnt/[beta]-catenin pathway was activated. Results On the 0th, 3rd, and 7th days of odontogenic differentiation of hDPSCs, SNHG1 showed a gradual up-regulation trend. SNHG1 overexpression enhanced the mRNA and protein expression of dentin sialophosphoprotein (DSPP), dentine matrix protein 1 (DMP-1) and ALP. We found that SNHG1 could bind to miR-328-3p. miR-328-3p inhibited the odontogenic differentiation of hDPSCs. Therefore, miR-328-3p mimics rescued the effect of SNHG1 overexpression on promoting odontogenic differentiation. In addition, SNHG1 inhibited Wnt/[beta]-catenin pathway via miR-328-3p in odontogenic differentiation of hDPSCs. Conclusion lncRNA SNHG1 inhibits Wnt/[beta]-catenin pathway through miR-328-3p and then promotes the odontogenic differentiation of hDPSCs. Keywords: lncRNA SNHG1, Odontogenic differentiation, hDPSCs, miR-328-3p, Wnt/[beta]-catenin</abstract><pub>BioMed Central Ltd</pub><doi>10.1186/s13287-022-02979-w</doi></addata></record>
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subjects Genetic research
Phosphatases
RNA
Stem cells
title lncRNA SNHG1 regulates odontogenic differentiation of human dental pulp stem cells via miR-328-3p/Wnt/[beta]-catenin pathway
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